Search

As a new energy material of environmental protection, biomass porous carbon material has been a research hotspot in recent years. In this paper, the porous carbon materials from lettuce leaves (LLs-temperature-proportional-activator) were prepared under different conditions, such as sintering temperature, the different activator, and the mass ratio of raw material and the activator, and the technological conditions were optimized through the discussion on their lithium storage performances. The results show that there are two broad and weak XRD peaks at 2θ=22°-26° and 2θ≈43° in each material, corresponding to the lattice plane (002) and (101), which indicates that the material is an amorphous carbon material with a certain degree of graphitization. In addition, the first discharge capacity of LLs-800-4R-K can reach 674.5 mAh/g. After 200 cycles, its discharge specific capacity can be maintained at 209.6 mAh /g, and the energy density is 146.8 Wh/kg. It illustrates that LLs-800-4R-K has good cycle performance and specific capacity. Thus, the optimum process conditions are as follows. The sintering temperature is at 800 ℃, KOH is used as activator, the mass ratio of raw material and the activator is 1:4.

C28H22ZnN6O5, triclinic, P1̅ (no. 2), a = 9.9400(9) Å, b = 10.1638(8) Å, c = 13.0867(11) Å, α = 97.678(7)°, β = 94.730(7)°, γ = 98.694(7)°, V = 1288.09(19) Å3, Z = 2, Rgt(F) = 0.0692, wRref(F2) = 0.1587, T = 293(2) K.

The paper introduced design schemes of whole structure, main hardware circuits and software of a novel mine-used intelligent water-pressure sensor based on STM32F103RBT6. The sensor adopts design way of low power consumption circuit and time-sharing power supply way to make power consumption be 0.006 mA under idle condition and 0.5 mA under collection and sending condition.

C19H15Br2MnN11, monoclinic, P21/m (no. 11), a = 8.442(2) Å, b = 15.478(3) Å, c = 9.266(2) Å, β = 111.54(3)°, V = 1126.3 Å3, Z = 2, Rgt(F) = 0.0568, wRref(F2) = 0.1554, T = 293 K.

Bromodomain PHD finger transcription factor (BPTF) is a core subunit of the nucleosome-remodeling factor (NURF) complex, which plays an important role in the development of several cancers. However, it is unknown whether BPTF regulates the progression of ovarian cancer (OC). To investigate this, we measured the relative expression levels of BPTF in OC cell lines and tissues using Western blot and immunohistochemistry, respectively, and the results were analyzed using the [chi-square] test. We also examined the effects from BPTF knockdown on the proliferation, migration, invasiveness, and apoptosis of OC cell lines. Mechanistic studies revealed that these effects were achieved through simultaneous modulation of multiple signaling pathways. We found that BPTF was highly expressed in OC cell lines and tissues compared with a normal human ovarian epithelial cell line and non-cancerous tissues (P < 0.05). These results are also supported by the public RNA-seq data. BPTF overexpression was correlated with a poor prognosis for OC patient survival (P < 0.05). In vitro experiments revealed that the downregulation of BPTF inhibited OC cell proliferation, colony formation, migration, and invasiveness, and induced apoptosis. BPTF knockdown also affected the epithelial-mesenchymal transition (EMT) signaling pathways and induced the cleavage of apoptosis-related proteins. Consequently, BPTF plays a critical role in OC cell survival, and functions as a potential therapeutic target for OC. Key words: BPTF, ovarian cancer, proliferation, survival. Le facteur de transcription BPTF (bromodomain PHD finger transcription factor) est une sous-unité centrale du complexe NURF (nucleosome remodeling factor), qui joue un rôle important dans le développement de plusieurs cancers. Toutefois, on ignore si BPTF régule la progression du cancer ovarien (CO). L'expression relative de BPTF dans les lignées cellulaires et les tissus de CO a été mesurée respectivement par Western blot et immunohistochimie. La signification clinique de BPTF dans le CO a été analysée par un test de [chi-square]. Les effets du knockdown de BPTF sur la prolifération, la migration, l'invasion et l'apoptose des cellules de CO ont été examinés. Des études sur les mécanismes ont révélé que ces effets étaient obtenus par la modulation simultanée de plusieurs voies de signalisation. Les auteurs ont constaté que BPTF était fortement exprimé dans les lignées cellulaires et les tissus de CO par rapport aux cellules épithéliales ovariennes humaines normales etauxtissus non cancéreux (P < 0,05). Ces résultats sont également étayés par les données publiques de séquençage de l'ARN. La surexpression de BPTF était corrélée à une faible survie des patientes atteintes d'un cancer de l'ovaire (P < 0,05). Des expériences in vitro ont révélé que la régulation à la baisse de BPTF inhibait la prolifération, la formation de colonies, la migration, l'invasion et induisait l'apoptose des cellules de CO. Le knockdown de BPTF régulait aussi les voies de signalisation de la transition épithélio-mésenchymateuse (TEM) et induisait le clivage de protéines liées à l'apoptose. Par conséquent, BPTF joue un rôle essentiel dans la régulation de la survie des cellules du CO et agit comme une cible thérapeutique potentielle pour le CO. [Traduit par la Rédaction] Mots-clés: BPTF, cancer de l'ovaire, prolifération, survie., Introduction According to the latest report in 2018, ovarian cancer (OC) ranks as the fifth highest cause of mortality due to cancer among females (Siegel et al. 2018). Epithelial ovarian [...]

Numerous studies have reported that CPSF4 is over-expressed ina large percentageofhuman lung cancers, and CPSF4 has been identified as a potential oncogene of human lung tumor. Downregulation of CPSF4 inhibits the proliferation and promotes the apoptosis of lung adenocarcinoma cells. A previous study by our group also found overexpression of CPSF4 in breast cancer (BC), and was closely associated with a poor prognosis for the patient. This study investigates microRNAs (miRNAs) that target CPSF4 to modulate BC cell proliferation. We found that miR-4458 was noticeably reduced in BC tissues and cells. Using a miR-4458 mimic, we found that cell proliferation, migration, and invasiveness were suppressed by miR-4458 overexpression, and were enhanced by reducing the expression of miR-4458. Moreover, the results from bioinformatics analyses suggest a putative target site in the CPSF4 3'-UTR. Furthermore, using luciferase reporter assays and Western blotting, we verified that miR-4458 directly targets the 3'-UTRofCPSF4 and downregulatesCOX-2andh-TERT, which are downstream target genesofCPSF4. Additionally, PI3K/AKT and ERK were shown to be inhibited by miR-4458 overexpression in BC cells. Moreover, miR-4458 suppresses BC cell growth in vivo. Consequently, these results suggest that the miR-4458--CPSF4--COX-2--hTERT axis might serve as a potential target for the treatment of BC patients. Key words: miR-4458, breast cancer, growth, migration, invasiveness, CPSF4. Plusieurs etudes ont suggere que CPSF4 soit surexprime dans un pourcentage important de cancers du poumon chez l'humain et elles l'ont identifie comme oncogene potentiel dans les tumeurs pulmonaires humaines. La regulation a la baisse de CPSF4 inhibait la proliferation des cellules d'adenocarcinome pulmonaire et favorisait leur apoptose. Les etudes anterieures realisees par les auteurs suggeraient que la surexpression de CPSF4 etait aussi observee dans le cancer du sein et qu'elle etait etroitement associee a un mauvais pronostic. Cette etude visait a identifier des microARN (miARN) d'interet qui cibleraient CPSF4 afin de moduler la proliferation des cellules de cancer du sein. Ils ont trouve que le miR-4458 etait particulierement reduit dans les tissus et les cellules de cancers mammaires. En utilisant un mime du miR-4458, la proliferation, la migration et l'invasion cellulaires etaient reprimees par la surexpression du miR-4458 alors qu'elles etaient accrues par la reduction du miR-4458. De plus, une analyse bioinformatique suggerait la presence d'un site cible presume dans la portion 3'-UTR de CPSF4. Par ailleurs, les auteurs ont verifie que le miR-4458 ciblait directement le 3'-UTR de CPSF4 a l'aide du dosage de l'activite du rapporteur luciferase et par buvardage de Western. Ils ont aussi montre qu'il regulait a la baisse COX-2 et h-TERT, qui sont des cibles en aval de CPSF4. En outre, PI3K/AKT et ERK s'averaient etre inhibees par la surexpression du miR-4458 dans les cellules de cancer du sein. Qui plus est, le miR-4458 reprimait la croissance cellulaire in vivo. En consequence, ces resultats suggerent que l'axe miR-4458--CPSF4--COX-2--hTERT pourrait agir comme cible potentielle dansletraitement depatientes atteintes d'un cancer du sein. [Traduit par la Redaction] Mots-cles : miR-4458, cancer du sein, croissance, migration, invasion, CPSF4., Introduction Breast cancer (BC) is one of the leading causes of death due to cancer among women worldwide (Chen et al. 2016; Siegel et al. 2017). Surgery, radiotherapy, chemotherapy, and [...]

BACKGROUND: Acute stroke poses a serious threat to people's health. The occurrence of a thrombus following the rupture of vulnerable plaques in the carotid artery is a significant contributor to the development of stroke. In previous case reports, it has been challenging to visualize tiny ulcerations within carotid artery plaques using computed tomography angiography (CTA) and digital subtraction angiography (DSA), even when the rupture of the plaque leads to the formation of a free-floating thrombus (FFT). However, in this particular case, contrast-enhanced ultrasound (CEUS) was able to overcome this limitation and provide a more precise assessment, confirming that the FFT formation was indeed a result of plaque rupture rather than any other potential causes. Cases that utilize CEUS to visualize the formation of ulcers and FFT resulting from plaque rupture are even more rare. As such, we present this case to shed light on this infrequent phenomenon. CASE SUMMARY: In this case study, we present a 65-year-old male patient who was admitted to the hospital due to headache and abnormal mental behavior for one day. During the routine cervical artery ultrasound examination upon admission, we detected the presence of plaque in the right internal carotid artery of the patient, resulting in luminal stenosis. Additionally, we observed suspected hypoechoic material at the distal end of the plaque. After undergoing CEUS examination, it was definitively determined that an ulcer had formed and a FFT had developed due to the rupture of carotid artery plaque. Subsequent CTA and DSA examinations further confirmed the presence of the FFT. The magnetic resonance imaging (MRI) reveals an acute lacunar infarction in the head of the right caput nuclei caudate, which strengthens the potential link between the patient's neurological and psychiatric symptoms observed during admission. The patient received prompt antiplatelet therapy and underwent cervical artery stenting surgery with the assistance of a distal embolic protection device. Following the procedure, the patient was discharged on the fourth day and experienced a complete recovery. CONCLUSION: CEUS is a valuable tool for visualizing FFT resulting from the rupture of vulnerable plaques in the carotid artery. [ABSTRACT FROM AUTHOR]

Current cancer therapies have encountered adverse response due to poor therapeutic efficiency, severe side effects and acquired resistance to multiple drugs. Thus, there are urgent needs for finding new cancer-targeted pharmacological strategies. In this review, we summarized the current understanding with THZ1, a covalent inhibitor of cyclin-dependent kinase 7 (CDK7), which demonstrated promising anti-tumor activity against different cancer types. By introducing the anti-tumor behaviors and the potential targets for different cancers, this review aims to provide more effective approaches to CDK7 inhibitor-based therapeutic agents and deeper insight into the diverse tumor proliferation mechanisms. Keywords: THZ1, Cyclin-dependent kinase 7, Cancer therapy, Transcription, Super-enhancer

Colorectal cancer (CRC) is a common malignant tumor that affects people worldwide. Metagenomic analyses have shown an enrichment of Fusobacterium nucleatum (F. nucleatum) in colorectal carcinoma tissue; many studies have indicated that F. nucleatum is closely related to the colorectal carcinogenesis. In this review, we provide the latest information to reveal the related molecular mechanisms. The known virulence factors of F. nucleatum promote adhesion to intestinal epithelial cells via FadA and Fap2. Besides, Fap2 also binds to immune cells causing immunosuppression. Furthermore, F. nucleatum recruits tumor-infiltrating immune cells, thus yielding a pro-inflammatory microenvironment, which promotes colorectal neoplasia progression. F. nucleatum was also found to potentiate CRC development through toll-like receptor 2 (TLR2)/toll-like receptor 4 (TLR4) signaling and microRNA (miRNA)-21 expression. In addition, F. nucleatum increases CRC recurrence along with chemoresistance by mediating a molecular network of miRNA-18a*, miRNA-4802, and autophagy components. Moreover, viable F. nucleatum was detected in mouse xenografts of human primary colorectal adenocarcinomas through successive passages. These findings indicated that an increased number of F. nucleatum in the tissues is a biomarker for the diagnosis and prognosis of CRC, and the underlying molecular mechanism can probably provide a potential intervention treatment strategy for patients with F. nucleatum-associated CRC. Keywords: Fusobacterium nucleatum, Colorectal carcinoma, Carcinogenesis, Immune microenvironment, Intervention therapy